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Differential modulation of alpha 3 beta 2 and alpha 3 beta 4 neuronal nicotinic receptors expressed in Xenopus oocytes by flufenamic acid and niflumic acid

R Zwart, M Oortgiesen and HP Vijverberg
Journal of Neuroscience 1 March 1995, 15 (3) 2168-2178; https://doi.org/10.1523/JNEUROSCI.15-03-02168.1995
R Zwart
Research Institute of Toxicology, Utrecht University, The Netherlands.
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M Oortgiesen
Research Institute of Toxicology, Utrecht University, The Netherlands.
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HP Vijverberg
Research Institute of Toxicology, Utrecht University, The Netherlands.
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Abstract

Effects of flufenamic acid (FFA) and niflumic acid (NFA), which are often used to block Ca(2+)-activated Cl- current, have been investigated in voltage-clamped Xenopus oocytes expressing alpha 3 beta 2 and alpha 3 beta 4 nicotinic ACh receptors (nAChRs). NFA and FFA inhibit alpha 3 beta 2 nAChR-mediated inward currents and potentiate alpha 3 beta 4 nAChR-mediated inward currents in normal, Cl(-)-free and Ca(2+)-free solutions to a similar extent. The concentration-dependence of the inhibition of alpha 3 beta 2 nAChR-mediated ion current yields IC50 values of 90 microM for FFA and of 260 microM for NFA. The potentiation of alpha 3 beta 4 nAChR-mediated ion current by NFA yields an EC50 value of 30 microM, whereas the effect of FFA does not saturate for concentrations of up to 1 mM. At 100 microM, FFA reduces the maximum of the concentration-effect curve of ACh for alpha 3 beta 2 nAChRs, but leaves the EC50 of ACh unaffected. The same concentration of FFA potentiates alpha 3 beta 4 nAChR-mediated ion currents for all ACh concentrations and causes a small shift of the concentration-effect curve of ACh to lower agonist concentrations. The potentiation, like the inhibition, is most likely due to a noncompetitive effect of FFA. Increasing ACh-induced inward current either by raising the agonist concentration from 10 microM to 200 microM or by coapplication of 10 microM ACh and 200 microM FFA causes a similar enhancement of block of the alpha 3 beta 4 nAChR-mediated ion current by Mg2+. This suggests that the effects of FFA and of an increased agonist concentration result in a similar functional modification of the alpha 3 beta 4 nAChR- operated ion channel. It is concluded that alpha 3 beta 4 and alpha 3 beta 2 nAChRs are oppositely modulated by FFA and NFA through a direct beta-subunit-dependent effect.

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The Journal of Neuroscience: 15 (3)
Journal of Neuroscience
Vol. 15, Issue 3
1 Mar 1995
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Differential modulation of alpha 3 beta 2 and alpha 3 beta 4 neuronal nicotinic receptors expressed in Xenopus oocytes by flufenamic acid and niflumic acid
R Zwart, M Oortgiesen, HP Vijverberg
Journal of Neuroscience 1 March 1995, 15 (3) 2168-2178; DOI: 10.1523/JNEUROSCI.15-03-02168.1995

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Differential modulation of alpha 3 beta 2 and alpha 3 beta 4 neuronal nicotinic receptors expressed in Xenopus oocytes by flufenamic acid and niflumic acid
R Zwart, M Oortgiesen, HP Vijverberg
Journal of Neuroscience 1 March 1995, 15 (3) 2168-2178; DOI: 10.1523/JNEUROSCI.15-03-02168.1995
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